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ديوان كانى (MS 384); منشأت (MS 385)
Birbirinden farklı 2 adet yazmanın bir araya getirilmesiyle oluşturulmuş ve ciltlenmiş bir eserdir (Yazma numaraları : MS 384, MS 385). Her iki yazma da Osmanlıca olup 1797 yılında yazılmıştır. MS 384 : 1b-2a: mensur dibace; 2b-9a: besmele manzumeleri, naatler ve tarikat pirlerine yazılan kasideler; 9b-30a: kasideler; 30a-35a: bir mecmuanın zahrına yazdıkları ebyat ve mersiyeler; 35a-41b: tarih manzumeleri; 41b-45a: musammatlar; 45a-91b: gazeller; 91b-99a: mukattaat; 99a-102b: ebyât. Ayrıca 1a’da bir beyit, kısa bir not ve okunamayan bir mühür, 1b’de Muhyiddin adına ikinci bir mühür vardır. Divanın sonunda şairin münşeatı (bkz. 230/II). Eserin tenkitli metni yayımlanmıştır (bkz. kaynakça). MS 385 : Eser bir çoğu mizahi bir vurgu taşıyan ve inşa üslubuyla yazılmış mektupların bir araya gelmesiyle oluşmuş bir derlemedir. İlk metin “sûret-i arzıhâl ez-cânib-i hod”, son metin “fıkra-i âher” başlığını taşır. Son sayfada Hüseyin adına mühür vardır
Data_Sheet_1_Effects of Aberrant miR-384-5p Expression on Learning and Memory in a Rat Model of Attention Deficit Hyperactivity Disorder.pdf
Attention deficit hyperactivity disorder (ADHD) is a common neuropsychiatric disorder characterized by inattention, hyperactivity, and impulsivity. It may be accompanied by learning difficulties and working memory deficits. Few studies have examined the role of miRNAs in cognitive dysfunction in ADHD. This study investigated the effects of aberrant miR-384-5p expression on learning and memory in a widely used ADHD rat model. Lentiviral vectors were injected into the lateral ventricles of the rats to increase or decrease miR-384-5p level. To determine whether aberrant miR-384-5p expression affects learning and memory, spontaneous activity and cognitive function were assessed with the open field and Morris water maze tests. In the place navigation experiment of the Morris water maze test, time, and total swimming distance to reach the platform decreased compared to the control group when miR-384-5p was overexpressed, whereas down-regulation of miR-384-5p had the opposite effect. There were no obvious changes in brain tissue morphology following miR-384-5p overexpression or inhibition; however, dopamine (DA) receptor D1 (DRD1) level has decreased and increased, respectively, in the prefrontal cortex (PFC). The luciferase activity of the wild-type DRD1 group has decreased in luciferase reporter assay. Cyclic AMP response element-binding protein (CREB) phosphorylation has increased, and DA transporter (DAT) level has decreased in the PFC of spontaneously hypertensive rats (SHR) by miR-384-5p overexpression. On the other hand, miR-384-5p suppression increased DRD1 and decreased DAT and CREB protein levels relative to control rats. These findings suggest that miR-384-5p may play a critical role in learning and memory impairment in ADHD.</p
miR-384-5p in Candida-induced acute lung injury
MiR-384-5p Regulates Inflammation in Candida-induced Acute Lung Injury by Downregulating PGC1β and Enhancing Candida-triggered Signaling Pathways</p
Bulletin No. 384 - Detergents for Scouring Grease Wools
Bulletin No. 384 - Detergents for Scouring Grease Wool
Gemeindenachrichten Ottensheim 2017 / 384 (2017 / 384)
GEMEINDENACHRICHTEN OTTENSHEIM 2017 / 384
Gemeindenachrichten Ottensheim (-)
Gemeindenachrichten Ottensheim 2017 / 384 (2017 / 384) ([2]
Resolución UNRN N° 384/2009. Designa docente interino.
Fil: Universidad Nacional de Río Negro (U). Universidad Nacional de Río Negro. Río Negro, ArgentinaResolución UNRN N° 384/2009. Designa docente interino.fals
Going Beyond Counting First Authors in Author Co-citation Analysis
The present study examines one of the fundamental aspects of author co-citation analysis (ACA) - the way co-citation
counts are defined. Co-citation counting provides the data on which all subsequent statistical analyses and mappings
are based, and we compare ACA results based on two different types of co-citation counting - the traditional type that
only counts the first one among a cited work's authors on the one hand and a non-traditional type that takes into
account the first 5 authors of a cited work on the other hand. Results indicate that the picture produced through this non-traditional author co-citation counting contains more coherent author groups and is therefore considerably clearer. However, this picture represents fewer specialties in the research field being studied than that produced through the traditional first-author co-citation counting when the same number of top-ranked authors is selected and analyzed. Reasons for these effects are discussed
Commentarii Collegii Conimbricensis, Societatis Iesv, In Qvatvor Libros De Coelo, Meteorologicos et Parua Naturalia, Aristotelis Stagiritae.
Data wyd. na s. tyt. w wersji rz.
Supplementary Material for: MicroRNA-384-5p Promotes Endothelial Progenitor Cell Proliferation and Angiogenesis in Cerebral Ischemic Stroke through the Delta-Likeligand 4-Mediated Notch Signaling Pathway
Background: MicroRNAs (miRs) have a crucial regulatory role in endothelial cell function and tumor angiogenesis by inhibiting the expressions of their target genes. The participation of microRNA-384-5p (miR-384-5p) has been prominently reported in various ischemia-induced diseases such as myocardial ischemia and atherosclerosis. Hence, the present study aimed at exploring the effect of miR-384-5p on proliferation, apoptosis, and angiogenesis of endothelial progenitor cells (EPCs) in cerebral ischemic stroke and investigating the associated underlying mechanism. Methods: A middle cerebral artery occlusion (MCAO) mouse model was established, with determination of the expression of cluster of differentiation 31 (CD31) and vascular endothelial growth factor (VEGF) proteins. Next, the MCAO mice and EPCs separated from MCAO mice were injected or transfected with mimics or inhibitors of miR-384-5p, or small interference RNA Delta-likeligand 4 (si-DLL4) in order to evaluate their effect on brain infarct size, cell proliferation, apoptosis, and angiogenesis. The relationship among miR-384-5p, DLL4, and the Notch signaling pathway was then verified by a series of experiments. Results: In MCAO mice, an increased brain infarct size and cell apoptosis in brain tissues were evident, with decreased expression of miR-384-5p, VEGF, and CD31, as well as increased DLL4 expression. After miR-384-5p mimic or si-DLL4 treatment, the brain infarct size and cell apoptosis in the brain tissues were reduced in compliance with an increased expression of VEGF and CD31. Our findings demonstrated that miR-384-5p negatively regulated the expression of DLL4, which further downregulated the Notch signaling pathway. When miR-384-5p was overexpressed or DLL4 silenced, the cell proliferation and angiogenesis of EPCs were promoted and cell apoptosis was inhibited. Conclusions: Our study demonstrated that overexpressed miR-384-5p targeting DLL4 could stimulate proliferation and angiogenesis, while inhibiting apoptosis of EPCs in mice with cerebral ischemic stroke through the Notch signaling pathway
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